项目名称: MSCs来源exosomes调控TGF―β/Smad信号通路介导的EMT在修复受损子宫内膜中的作用及机制
项目编号: No.81460225
项目类型: 地区科学基金项目
立项/批准年度: 2015
项目学科: 医药、卫生
项目作者: 刘芳
作者单位: 石河子大学
项目金额: 48万元
中文摘要: 子宫内膜损伤后修复障碍是月经过少、宫腔粘连、闭经及继发不孕的重要病因。 MSCs来源Exo因其在纤维化疾病中的调节作用而备受关注。项目组前期发现:动物实验中损伤子宫内膜发生EMT,TGF-β mRNA水平和Smad蛋白表达上调,初步证实TGF-β/Smad信号通路可能调控EMT参与子宫内膜损伤;而移植MSCs对子宫内膜损伤模型有显著的修复作用。本研究拟:通过体内外实验模型证实TGF-β/Smad信号通路介导EMT促进子宫内膜损伤的作用机制,将PKH26荧光标记的MSCs来源Exo移植入子宫内膜损伤的新西兰兔体内,追踪Exo迁移,并检测Exo调控TGF-β /Smad信号通路介导的EMT,证实Exo促进受损子宫内膜修复的分子机制。通过本课题研究为阐明子宫内膜损伤发病机制、探寻治疗新方向提供理论基础。
中文关键词: 子宫内膜;损伤修复;间充质干细胞;exosomes;TGF―β/Smad信号通路
英文摘要: Endometrial repair disorder after injury is the important cause of hypomenorrhea, intrauterine adhesions, amenorrhea and secondary infertility. Exo derived from MSCs play a significant regulatory role in the fibrotic diseases. Earlier stage of project terms detected that: EMT occurred in endometrial injury in animal experiments, the levels of TGF-Β mRNA and the expression of Smad upregulated, and that initially confirmed TGF-β/Smad signaling pathway might regulated EMT involved in endometrial injury. The transplantion of MSCs promoted the repair of endometrial injury. The study intends to: confirm the mechanism of EMT induced by the TGF-β/Smad signaling pathway promoting endometrial injury by in vitro and in vivo experiments, and transplant the Exo derived from MSCs and labeled with PKH26 into the animal model of endometrial injury, and trace the migration of Exo , and detect the regulation of Exo to EMT induced by the TGF-β/Smad signaling pathway ,and prove the mechanism of Exo promoting to the repair of endometrial injury. The research will provide the theoretical basis for elucidating the pathogenesis of endometrial injury and explore the new therapeutic strategies.
英文关键词: endometrium;injury and repair;MSCs;exosomes;TGF-beta/Smad singaling pathway